Event Title

MB1 -- Does L-Methylfolate alleviate changes in autophagy induced by excess folic acid?

Location

URC Greatroom

Start Date

8-4-2022 10:30 AM

End Date

8-4-2022 12:15 PM

Description

Autism is a neurodevelopment disorder with several known causes in the realm of possible mutations that can lead to this condition. Autism now is known to have an epigenetic or environmental component as well. Folic acid is a dietary factor that affects epigenetics and was previously shown in our lab to lead to an increased number of dendritic spines in a human neuronal cell line (SHSY5Y cells). Increased dendritic spines is a distinctive phenotype of autism patients’ cortical brain tissues along with a reduction in autophagy rates. With this, the mutation of Methylenetetrahydrofolate reductase gene (MTHFR) is detrimental to neurological development as this gene plays a large role in regulation of the single carbon metabolism pathway. Mutations in MTHFR are common in autism patients. It is thought that excess Folic acid intake can lead to an increased risk of development of autism. L-Methylfolate is a folate form commonly used for treatment in Depression and Schizophrenia and shares association with folic acid in that it is an active derivative of folic acid just beyond the metabolic step that utilizes the MTHFR enzyme. Previously, our lab treated a human neuronal cell line with a 2x folic acid dose (48 hours) followed by another 48 hour folic acid treatment or a 48 hour L-Methylfolate treatment. L-Methylfolate alone showed no negative effects on dendritic spines or autophagy rates. When L-Methylfolate followed a 48 hour folic acid treatment, L-Methylfolate corrected excess dendritic spines and loss of autophagy induced by the 2x folic acid treatment. I hypothesized that following excessive folic acid consumption, L-Methylfolate could act as a counter to the detrimental effects caused by the folic acid. The molecular mechanism was not elucidated in previous studies, so here, we present Western Blotting data to indicate levels of autophagy pathway proteins after folic acid treatment followed by further Folic acid treatment or L-Methylfolate treatment.

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Apr 8th, 10:30 AM Apr 8th, 12:15 PM

MB1 -- Does L-Methylfolate alleviate changes in autophagy induced by excess folic acid?

URC Greatroom

Autism is a neurodevelopment disorder with several known causes in the realm of possible mutations that can lead to this condition. Autism now is known to have an epigenetic or environmental component as well. Folic acid is a dietary factor that affects epigenetics and was previously shown in our lab to lead to an increased number of dendritic spines in a human neuronal cell line (SHSY5Y cells). Increased dendritic spines is a distinctive phenotype of autism patients’ cortical brain tissues along with a reduction in autophagy rates. With this, the mutation of Methylenetetrahydrofolate reductase gene (MTHFR) is detrimental to neurological development as this gene plays a large role in regulation of the single carbon metabolism pathway. Mutations in MTHFR are common in autism patients. It is thought that excess Folic acid intake can lead to an increased risk of development of autism. L-Methylfolate is a folate form commonly used for treatment in Depression and Schizophrenia and shares association with folic acid in that it is an active derivative of folic acid just beyond the metabolic step that utilizes the MTHFR enzyme. Previously, our lab treated a human neuronal cell line with a 2x folic acid dose (48 hours) followed by another 48 hour folic acid treatment or a 48 hour L-Methylfolate treatment. L-Methylfolate alone showed no negative effects on dendritic spines or autophagy rates. When L-Methylfolate followed a 48 hour folic acid treatment, L-Methylfolate corrected excess dendritic spines and loss of autophagy induced by the 2x folic acid treatment. I hypothesized that following excessive folic acid consumption, L-Methylfolate could act as a counter to the detrimental effects caused by the folic acid. The molecular mechanism was not elucidated in previous studies, so here, we present Western Blotting data to indicate levels of autophagy pathway proteins after folic acid treatment followed by further Folic acid treatment or L-Methylfolate treatment.